Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA280950 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:BCR repertoire analysis of B cells from wild type, miR-17~92 Tg and miR-17~92 CD19Cre tKO mice
| PRJNA322560 | ENA
Project description:Ribosome Profiling analysis of Follicular B (FoB) cells purified from WT, miR-17~92 transgenic and miR-17-92 tKO mice
| PRJNA326723 | ENA
Project description:Knockout of the ubiquitously expressed microRNA-17~92 cluster in mice produces a lethal developmental lung defect. We validated the equally widely expressed pro-apoptotic Bim gene as joint target of miR-17~92 cluster members. To study the contribution of miR-17~92:Bim interaction to miR-17~92 overall function, we set up a system of conditional mutagenesis of the Bim 3’UTR. Blocking miR-17~92:Bim interaction early in development phenocopied the lethal lung phenotype of miR-17~92 ablation. Thus, despite hundreds of overall predicted targets vital miRNA functions can be mediated by a single target gene.
2019-11-10 | GSE123671 | GEO
Project description:To identify mir-17~92 targets in MNs, a set of target candidate genes from the intersection of upregulated genes found only in the mir-17~92 KO MNs that were predicted to be direct targets of mir-17~92 by TargetScan.
2015-04-14 | GSE67795 | GEO
Project description:miR-17-92 mediates the MYC oncogene addiction in a conditional mouse lymphoma model. To identify targets of miR-17-92 in this model, miR-17-92 was expressed in the conditional lymphoma cell lines using MSCV-puro.
2014-05-29 | GSE57507 | GEO
Project description:miR-17 from the miR-17-92 cluster regulate activation-induced cell death in T cells and modulate inducible regulatory T cell differentiation. We used microarrays to detail the global program of gene expression modulated by miR-17 and aim to identify the potential targets of miR-17. CD4 T cells from wild type or miR-17-92 deficient mice were activated and transduced with empty vector or that overexpressing miR-17. Potential targets of miR-17 should be upregulated in miR-17-92 deficient CD4 T cells compared to wild type CD4 T cells, and downregulated when miR-17 were reintroduced into the miR-17-92 deficient T cells.
2011-09-30 | E-GEOD-32533 | biostudies-arrayexpress
Project description:Knockout of the ubiquitously expressed microRNA-17~92 cluster in mice produces a lethal developmental defect and blocked B lymphopoiesis. We validated the equally widely expressed Bcl2l11 gene as joint target of miR-17~92 cluster members. Bcl2l11 encodes the pro-apoptotic protein BIM, central to life-death decisions in most mammalian cells. To study the contribution of miR-17~92:Bim interaction to miR-17~92 overall function, we set up a system of conditional mutagenesis of the Bim 3’UTR in the mouse. Blocking miR-17~92:Bim interaction early in development phenocopied the lethal developmental defect of miR-17~92 ablation. In contrast, hematopoietic and B lineage specific mutagenesis, while selectively compromising B lineage cell fitness, left hematopoietic cell compartments untouched as long as the cells expressed Bim biallelically. Thus, despite hundreds of overall predicted targets vital miRNA functions can be mediated by a single target gene, depending on cellular context and level of target gene expression.
2019-11-13 | GSE123672 | GEO
Project description:A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes for six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.
2021-09-09 | PXD018052 | Pride
Project description:The miR-17-92 cluster targets mRNAs involved in distinct pathways which either promote or inhibit tumor progression. However, the cellular and molecular mechanisms underlying miR-17~92 cluster mediated pro- or anti- tumorigenic effects has not been studied. In this study, we found that inhibition of colon cancer progression is dictated by quantitatively controlling expression of the miR-17~92 cluster. To identify molecular mechanisms giving rise to the different growth/metastasis patterns, we profiled gene expression in miR-Ctrl, miR-17~92Med and miR-17~92Hi cells using Affymetrix Murine GeneST Arrays.
2014-06-01 | GSE55631 | GEO
Project description:Differential gene expression in nephron progenitors lacking miR-17~92
| PRJNA229148 | ENA